XPF Inhibitors

XPF inhibitors constitute a class of chemicals that affect the function of the XPF protein, primarily by modulating various DNA repair pathways. These inhibitors include compounds such as Cisplatin, Methyl methanesulfonate, Doxorubicin, Olaparib, Vorinostat, Camptothecin, ATM kinase inhibitors (e.g., KU-55933), VE-821, DNA-PK inhibitors (e.g., NU7441), AZD7762, Hydroxyurea, and H2O2. XPF, a crucial component of the nucleotide excision repair pathway, plays a pivotal role in maintaining genomic integrity by repairing DNA lesions induced by various sources of damage.

Cisplatin forms DNA adducts, resulting in DNA damage that activates DNA repair mechanisms, including nucleotide excision repair. This activation can indirectly affect XPF by engaging it in the repair process. Methyl methanesulfonate, DNA intercalators like Doxorubicin, and other agents that promote DNA damage trigger repair responses that indirectly involve XPF. Olaparib, a PARP inhibitor, blocks DNA repair, disrupting XPF's participation in DNA repair pathways. Histone deacetylase inhibitors like Vorinostat influence chromatin structure and gene expression, indirectly affecting DNA repair pathways involving XPF. Inhibitors of topoisomerases, such as Camptothecin, induce DNA damage, triggering DNA repair responses that may involve XPF indirectly. Inhibition of ATM kinase with compounds like KU-55933 disrupts the DNA damage response, affecting XPF's role in DNA repair. VE-821, an inhibitor of ATR kinase, interferes with the DNA damage checkpoint and DNA repair processes, impacting XPF function. DNA-PK inhibitors, such as NU7441, hinder non-homologous end joining (NHEJ) repair, indirectly affecting XPF-related DNA repair pathways. AZD7762 and Hydroxyurea disrupt cell cycle checkpoints and DNA repair responses, influencing XPF-mediated repair mechanisms. Additionally, reactive oxygen species (ROS), like H2O2, can cause DNA damage and activate repair pathways, involving XPF indirectly.